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Abstract
Accidental intravascular administration of bupivacaine duringperformance of a brachial block precipitated convulsions followedby asystole. The patient was rapidly resuscitated using cardiopulmonaryresuscitation, supplemented by 150 mL of 20% lipid emulsion.Nonetheless, cardiac toxicity reappeared 40 min after completionof the lipid emulsion. In the absence of further lipid emulsion,amiodarone and inotropic support were used to treat cardiotoxicity.This case suggests that local anesthetic systemic toxicity mayrecur after initial lipid rescue. Since recurrence of toxicitymay necessitate administration of additional doses of lipidemulsion, a sufficient quantity of lipid emulsion should beavailable when regional anesthesia is performed.
The use of lipid emulsions to treat systemic local anesthetictoxicity has recently been highlighted in case reports1–9and editorials.10–16 We present a case of lipid rescuein which systemic toxicity recurred 40 min after successfultreatment with lipid emulsion.

A single injection infraclavicular paracoracoid block was performedafter placement of an 18-gauge ported IV cannula. No sedationwas administered. The brachial plexus was located using a 50mm insulated needle (Stimuplex®, B Braun, Melsungen, Germany)attached to a nerve stimulator (Neuro-Trace III®, HDC®Corporation, Milpitas, CA). Evoked responses of finger and wristflexion were first elicited at 2 mA and disappeared at 0.4 mA.After injection of 30 mL of 0.375% bupivacaine hydrochloridewithout epinephrine (Micro Healthcare, Bethlehem, South Africa)over 3 min, with aspiration at 5 mL intervals, the patient abruptlyreported the new onset of a dry sensation in his throat andeyes. These symptoms prompted immediate cessation of local anestheticinjection and removal of the insulated needle. This was immediatelyfollowed by generalized convulsions and apnea. Facemask intermittentpositive pressure ventilation delivering 100% oxygen was initiated.Intralipid® (Fresenius Kabi®, South Africa) that washeld in the postanesthesia care unit was available within 30s of the onset of convulsions. Convulsions were terminated within60 s by the administration of IV thiopental, 100 mg succeededby a further 150 mg.

After termination of convulsions, the electrocardiogram tracebecame visible and revealed a narrow complex tachycardia, whichaccelerated to a peak rate of 160 bpm. Over 90 s, the tachycardiawas succeeded by broadening of the QRS complexes, slowing ofthe heart rate and asystole.

Over the 30 min after return of spontaneous circulation, theremaining 350 mL contained in the Intralipid bag were infused.During this time, his heart rate and rhythm reverted to sinustachycardia at 110 bpm. The circulation was supported with anepinephrine infusion that was progressively decreased to 0.06µg · kg–1 · min–1 at this time.

The patient remained hemodynamically stable and, at the endof this 30 min period, it was decided by the anesthesiologistand surgeon to proceed with the planned debridement. This wasfacilitated by administering a 5 mg bolus of midazolam and isoflurane(end-tidal partial pressure 0.5 kPa). The debridement was completedwithin 10 min.

After surgery, the patient remained in the operating room untilintensive care unit admission was possible. However, at theend of the next 30 min period, (approximately 40 min after theconclusion of Intralipid infusion), a progressively acceleratingsinus tachycardia at a rate of 140 bpm, accompanied with frequentmultifocal ventricular extrasystoles and short, self-terminatingruns of ventricular tachycardia were observed. In view of whatwas presumed to be the recurrence of bupivacaine cardiotoxicity,additional Intralipid was ordered. However, the recovery room’semergency stock was comprised of only one 500 mL bag which hadnow been used and no additional Intralipid could be obtainedfor several hours. Therefore, an amiodarone initial loadingdose of 300 mg in 200 mL of 5% dextrose was infused over 30min.

Admission to the intensive care unit took place 1 h after completionof the amiodarone loading dose by which time the arrhythmiashad terminated and inotropic support was discontinued. The patientwas tracheally extubated 5 h after his initial episode of systemictoxicity. Despite an initial serum amylase concentration of608 IU/L, no clinical signs of pancreatitis were noted. On thefirst postarrest day, total creatine kinase of 2378 IU/L, MBfraction 26 µg/L and Troponin I 1.255 µg/L suggestedthat myocardial damage had occurred. Four days later, cardiacenzyme levels decreased to 765 IU/L, 1.1 µg/L and 0.059µg/L, respectively. Hospital discharge occurred 4 daysafter the initial event.

DISCUSSION
The outstanding feature of this case was the recurrence of cardiovascularinstability 40 min after completion of Intralipid administrationfor bupivacaine cardiotoxicity. We attributed the cardiovascularinstability to recurrence of local anesthetic toxicity afterlipid rescue, a scenario not previously described. The causeof recurrence of toxicity was likely multifactorial. The serumconcentration of Intralipid would have decreased due to redistributionand metabolism. The elimination half-life of IV bupivacaineis longer than all other currently used local anesthetics, reportedly3.5 h.17 This may have been prolonged because of poor hepaticfunction and perfusion in the aftermath of the cardiac arrest.Bupivacaine may have redistributed back into the central compartment.Initial tissue entry and subsequent acidosis-related ion trapping,17with later release into the plasma as the acidosis resolved,would have increased the plasma concentrations of bupivacaine.Furthermore, pulmonary uptake of local anesthetics decreasesarterial concentrations by 20%; subsequent release of localanesthetic occurs over an unknown time, in an exponentiallydecreasing manner.18

For treatment of local anesthetic toxicity, both the Associationof Anesthetists of Great Britain and Ireland (AAGBI)19 and Weinberg20–22currently recommend an initial bolus of 1.5 mL/kg of 20% lipidemulsion administered over 1 min. This bolus may be repeatedtwice at 5 min intervals if an adequate circulation has notbeen restored. The bolus should be followed by an infusion of0.25 to 0.5 mL · kg–1 · min–1, theAAGBI recommending administration over 20 min, whereas Weinbergrecommends the infusion be continued for 30 min. Weinberg suggeststhat a total dose exceeding 8 mL/kg 20% lipid emulsion is notlikely to be needed.21,22 These recommendations imply that asingle 500 mL bag will suffice for most 60–70 kg patients.However, our case lends support to the AAGBI recommendationthat at least 1000 mL 20% lipid emulsion should be available.23,24

The postoperative increase in serum amylase could indicate pancreaticinjury. While pancreatitis is a known complication of chronichyperlipidemia,25 the significance of the hyperamylasemia seenin our patient is currently unclear. Although we cannot findanother documented increase in amylase or pancreatic injuryafter the use of lipid emulsion in resuscitation, this issuemust be considered after lipid rescue.

In summary, we report a case of recurrent systemic local anesthetictoxicity after successful treatment with lipid emulsion. Becauseno additional lipid emulsion was available, the recurrent dysrhythmiaswere treated with amiodarone. This case documents the importanceof the availability of a sufficient quantity of lipid emulsionwhen regional anesthesia is performed.Footnotes
Accepted for publication November 24, 2008.
Reprints will not be available from the author.REFERENCES

The Association of Anaesthetists of Great Britain & Ireland 2007. The Association of Anaesthetists of Great Britain & Ireland 2007, Guidelines for the Management of Severe Local Anaesthetic Toxicity. http://www.aagbi.org/publications/gu...toxicity07.pdf. 2007; accessed July 23, 2008.